The Experts below are selected from a list of 159 Experts worldwide ranked by ideXlab platform
Boqiang Wu - One of the best experts on this subject based on the ideXlab platform.
-
An Energy Metering and Measurement SoC With a Novel Low-Power DSP Architecture
IEEE Internet of Things Journal, 2019Co-Authors: Boqiang WuAbstract:This paper presents an energy metering and measurement system-on-a-chip (SoC) with a novel low-power digital signal processor (DSP) architecture. The Cotex-M0-based SoC can measure electricity signals and meter active and reactive energy. It can also monitor the grid by directly accessing and analyzing the waveforms. The measurement and metering algorithms are implemented in a novel DSP architecture with a dedicated reduced instruction set. The filter coefficients and its operating frequency in the Default Program of DSP can be reProgrammed independently. It can be applied in different applications where demands for metering bandwidth and response time are different. The DSP Program can also be reProgrammed by the software if the Default Program is not desired. The SoC is implemented in a 0.11- ${\mu }\text{m}$ CMOS process. It achieves active and reactive energy metering accuracy of 0.1% with a dynamic range of 5000:1. The analog power supply is 3.3 V and the digital power supply is 1.8 V. The total power consumption of the SoC is ca 17.63 mW with the DSP consuming ca 1.0 mW. Compared with other commercial metering and measurement SoCs, the presented SoC achieves higher metering accuracy and lower power consumption. It is currently in production.
-
An Energy Metering and Measurement SoC With a Novel Low-Power DSP Architecture
IEEE Internet of Things Journal, 2019Co-Authors: Boqiang WuAbstract:This paper presents an energy metering and measurement system-on-a-chip (SoC) with a novel low-power digital signal processor (DSP) architecture. The Cotex-M0-based SoC can measure electricity signals and meter active and reactive energy. It can also monitor the grid by directly accessing and analyzing the waveforms. The measurement and metering algorithms are implemented in a novel DSP architecture with a dedicated reduced instruction set. The filter coefficients and its operating frequency in the Default Program of DSP can be reProgrammed independently. It can be applied in different applications where demands for metering bandwidth and response time are different. The DSP Program can also be reProgrammed by the software if the Default Program is not desired. The SoC is implemented in a 0.11-μm CMOS process. It achieves active and reactive energy metering accuracy of 0.1% with a dynamic range of 5000:1. The analog power supply is 3.3 V and the digital power supply is 1.8 V. The total power consumption of the SoC is ca 17.63 mW with the DSP consuming ca 1.0 mW. Compared with other commercial metering and measurement SoCs, the presented SoC achieves higher metering accuracy and lower power consumption. It is currently in production.
Laurent Peres - One of the best experts on this subject based on the ideXlab platform.
-
differentiation Clearance of PML/RARA-bound promoters suffice to initiate APL
2020Co-Authors: Morgane Le Bras, Julien Ablain, Daniel Metzger, Laurent PeresAbstract:Abstract PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the RXRA co-receptor to PML/RARA is required for transformation, RXRA promoting its efficient DNA-binding. APL is exquisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiation . While RA elicits in vivotranscriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Here we demonstrate that extinction of PML/RARA triggers terminal differentiation in vivo . Similarly, ablation of RXRs loosens PML/RARA DNA-binding, inducing terminal differentiation of APL cells ex vivo or in vivo . RXRA sumoylation also directly contributes to PML/RARA-dependent transformation , presumably by enhancing transcriptional ex vivorepression. Thus, APL differentiation is a Default Program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.
-
Clearance of PML/RARA-bound promoters suffice to initiate APL differentiation.
Blood, 2014Co-Authors: Adeline Vitaliano-prunier, Juliane Halftermeyer, Julien Ablain, Aurélien De Reyniès, Laurent Peres, Morgane Le Bras, Daniel MetzgerAbstract:PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the RXRA co-receptor to PML/RARA is required for transformation, RXRA promoting its efficient DNA-binding. APL is exquisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiation in vivo. While RA elicits transcriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Here we demonstrate that extinction of PML/RARA triggers terminal differentiation in vivo. Similarly, ablation of RXRs loosens PML/RARA DNA-binding, inducing terminal differentiation of APL cells ex vivo or in vivo. RXRA sumoylation also directly contributes to PML/RARA-dependent transformation ex vivo, presumably by enhancing transcriptional repression. Thus, APL differentiation is a Default Program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.
Daniel Metzger - One of the best experts on this subject based on the ideXlab platform.
-
differentiation Clearance of PML/RARA-bound promoters suffice to initiate APL
2020Co-Authors: Morgane Le Bras, Julien Ablain, Daniel Metzger, Laurent PeresAbstract:Abstract PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the RXRA co-receptor to PML/RARA is required for transformation, RXRA promoting its efficient DNA-binding. APL is exquisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiation . While RA elicits in vivotranscriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Here we demonstrate that extinction of PML/RARA triggers terminal differentiation in vivo . Similarly, ablation of RXRs loosens PML/RARA DNA-binding, inducing terminal differentiation of APL cells ex vivo or in vivo . RXRA sumoylation also directly contributes to PML/RARA-dependent transformation , presumably by enhancing transcriptional ex vivorepression. Thus, APL differentiation is a Default Program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.
-
Clearance of PML/RARA-bound promoters suffice to initiate APL differentiation.
Blood, 2014Co-Authors: Adeline Vitaliano-prunier, Juliane Halftermeyer, Julien Ablain, Aurélien De Reyniès, Laurent Peres, Morgane Le Bras, Daniel MetzgerAbstract:PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the RXRA co-receptor to PML/RARA is required for transformation, RXRA promoting its efficient DNA-binding. APL is exquisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiation in vivo. While RA elicits transcriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Here we demonstrate that extinction of PML/RARA triggers terminal differentiation in vivo. Similarly, ablation of RXRs loosens PML/RARA DNA-binding, inducing terminal differentiation of APL cells ex vivo or in vivo. RXRA sumoylation also directly contributes to PML/RARA-dependent transformation ex vivo, presumably by enhancing transcriptional repression. Thus, APL differentiation is a Default Program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.
Antoon F. M. Moorman - One of the best experts on this subject based on the ideXlab platform.
-
Molecular pathway for the localized formation of the sinoatrial node
Circulation Research, 2007Co-Authors: Mathilda T.m. Mommersteeg, Danielle E W Clout, Willem M H Hoogaars, Virginia E. Papaioannou, Cornelia Wiese, Nigel A. Brown, Owen W.j. Prall, Corrie De Gier-de Vries, Richard P. Harvey, Antoon F. M. MoormanAbstract:The sinoatrial node, which resides at the junction of the right atrium and the superior caval vein, contains specialized myocardial cells that initiate the heart beat. Despite this fundamental role in heart function, the embryonic origin and mechanisms of localized formation of the sinoatrial node have not been defined. Here we show that subsequent to the formation of the Nkx2-5-positive heart tube, cells bordering the inflow tract of the heart tube give rise to the Nkx2-5-negative myocardial cells of the sinoatrial node and the sinus horns. Using genetic models, we show that as the myocardium of the heart tube matures, Nkx2-5 suppresses pacemaker channel gene Hcn4 and T-box transcription factor gene Tbx3, thereby enforcing a progressive confinement of their expression to the forming Nkx2-5-negative sinoatrial node and sinus horns. Thus, Nkx2-5 is essential for establishing a gene expression border between the atrium and sinoatrial node. Tbx3 was found to suppress chamber differentiation, providing an additional mechanism by which the Tbx3-positive sinoatrial node is shielded from differentiating into atrial myocardium. Pitx2c-deficient fetuses form sinoatrial nodes with indistinguishable molecular signatures at both the right and left sinuatrial junction, indicating that Pitx2c functions within the left/right pathway to suppress a Default Program for sinuatrial node formation on the left. Our molecular pathway provides a mechanism for how pacemaker activity becomes progressively relegated to the most recently added components of the venous pole of the heart and, ultimately, to the junction of the right atrium and superior caval vein.
Morgane Le Bras - One of the best experts on this subject based on the ideXlab platform.
-
differentiation Clearance of PML/RARA-bound promoters suffice to initiate APL
2020Co-Authors: Morgane Le Bras, Julien Ablain, Daniel Metzger, Laurent PeresAbstract:Abstract PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the RXRA co-receptor to PML/RARA is required for transformation, RXRA promoting its efficient DNA-binding. APL is exquisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiation . While RA elicits in vivotranscriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Here we demonstrate that extinction of PML/RARA triggers terminal differentiation in vivo . Similarly, ablation of RXRs loosens PML/RARA DNA-binding, inducing terminal differentiation of APL cells ex vivo or in vivo . RXRA sumoylation also directly contributes to PML/RARA-dependent transformation , presumably by enhancing transcriptional ex vivorepression. Thus, APL differentiation is a Default Program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.
-
Clearance of PML/RARA-bound promoters suffice to initiate APL differentiation.
Blood, 2014Co-Authors: Adeline Vitaliano-prunier, Juliane Halftermeyer, Julien Ablain, Aurélien De Reyniès, Laurent Peres, Morgane Le Bras, Daniel MetzgerAbstract:PML/RARA, a potent transcriptional inhibitor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyelocytic leukemia (APL). Association of the RXRA co-receptor to PML/RARA is required for transformation, RXRA promoting its efficient DNA-binding. APL is exquisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiation in vivo. While RA elicits transcriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Here we demonstrate that extinction of PML/RARA triggers terminal differentiation in vivo. Similarly, ablation of RXRs loosens PML/RARA DNA-binding, inducing terminal differentiation of APL cells ex vivo or in vivo. RXRA sumoylation also directly contributes to PML/RARA-dependent transformation ex vivo, presumably by enhancing transcriptional repression. Thus, APL differentiation is a Default Program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.
